The lessons science and pharmacology teach us about
achieving optimal health, vitality and maximal lifespan with a low net carb, high saturated fat, evolutionarily paleolithic-styled diet aligned with my ancestral heritage and how I lost 50 pounds of body fat. A sorta fairy story.

In the previous entry, conclusions from the same research below was discussed. They went further and looked at the lipoprotein subfractions including HDL2b and HDL3c. Mensink et al found that the higher the phospholipid transfer protein (PLTP) activity and the lower the cholesterol ester transfer protein (CETP) activity, the higher the relative abundance of HDL2b, the regression particle, and the lower the HDL3c, a small dense atherogenic particle. Lauric acid produced the highest ratio of PLTP to CETP activity when compared with the control, palmitic or oleic diets after 6-weeks.

Their assessment was "It is now clearly established that CETP and PLTP can modulate the size distribution of serum lipoprotein fractions. On the one hand, CETP can replace lipoprotein cholesteryl esters by hydrolyzable triglycerides which are derived from the triglyceride-rich lipoproteins, favoring the emergence of small-sized LDL, pre-beta-HDL and small-sized alpha-HDL [40]. On the otherhand, PLTP has been shown to promote the formation of both pre-beta-HDL and large-sized alpha-HDL through an inter-HDL fusional mechanism [40]. In the present study, no significant differences in the size distribution of either HDL or LDL fractions were observed in sera from subjects consuming either of the three experimental diets... Despite the absence of modifications of the size distribution of HDL, significant relationships between lipid transfer activities andthe relative abundance of HDL subpopulations were observed among (INDIVIDUAL) subjects consuming the same, standardized diet. Overall, CETP correlated positively with small HDL, but negatively with large HDL, whereas opposite tendencies were observed with PLTP that correlated negatively with small HDL, but positively with the large ones (ie, HDL2b)."

Minimization and maximization, respectively, as the Mensink study showed.

What are the dangers of artificially inhibiting CETP and ignoring PLTP activity?

What are the dangers of raising only HDL3c (small dense atherogenic HDL) and lowering HDL2b (the regressive, large/fluffy HDL)??!

The story of Torcetrapib...is one with an extremely unhappy unending...

Well...for one Pfizer is now out of the lipid-heart-disease business (Lipitor® RIP 2011 when it goes generic). Read the TYP report on this CETP-inhibitor and the surprising outcome HERE. Pfizer's $20B Torcetrapib HDL-raising drug unfortunately failed big time (in low-fat, low cholesterol, low saturated fat populations). Not only was an increase of 50% in total HDL observed in humans but also coronary regression was demonstrated in animal studies. Oddly this curious drug was associated with nearly double the deaths in the single human morbidity/mortality trial. Are animal brains as functional or large as human brains? What is the purpose of cholesterol? Are humans brains not laden with cholesterol? In fact 23% of the whole body pool of cholesterol is found in the brain and central nervous system. Although the brain only weighs 2.1% of our total weight, the cholesterol content is the highest compared with any other tissue (23 mg chol/gram). How much cholesterol is in an egg yolk? A measly ~200 mg. Barely enough to support or maintain a smidgeon of your SUPER SAVANT BRAIN. And we're told to have no more than an egg a day? Can you spell autism? Well... probably neither can the great-grandchildren of the geniuses who proposed these low-cholesterol indictments. How many more generations will be affected by the policies propagating the low-fat hypothesis? Are we de-evolving as a species *hint....WALL*E *?

Thematic review series: Brain Lipids. Cholesterol metabolism in the central nervous system during early development and in the mature animal. Journal of Lipid Research, Vol. 45, 1375-1397, August 2004.

BIOACTIVE LIPIDS -- BEST BALANCE -- BETTER THAN Torcetrapib

Fish oil EPA + DHA and seafood naturally lower CETP activity (preventing cholesterol transfer) and power up PLTP (moving phospholipids out of lipoprotein fractions). I had a hard time locating any VAP/NMR data on effects of fish oil components EPA and DHA, but two studies below demonstrate the outcome of EPA and DHA ingestion in depleting phospholipids out of LDL and HDL particles.

Native Chukot Peninsula residents, in contrast to Muscovites, consume a diet rich in n-3 polyunsaturated fatty acids. This dietary peculiarity is reflected in differences in plasma lipid and apolipoprotein contents. The Chukot residents have lower contents of total cholesterol, triglyceride, LDL (low density lipoprotein) cholesterol and apolipoprotein B, but higher HDL (high density lipoprotein) cholesterol levels than do Muscovites. The apolipoprotein A-I levels were identical in both groups. A higher HDL cholesterol to apolipoprotein A-I ratio was determined in the coastline Chukot residents (0.52 +/- 0.01) than in Muscovites (0.43 +/- 0.01; p less than 0.01). In contrast to Muscovites, the coastline Chukot residents also had higher n-3 and lower n-6 polyunsaturated fatty acid percentages in plasma and erythrocyte lipids, and lower phosphatidylcholine and higher sphingomyelin or phosphatidylethanolaminelevels in HDL2b and HDL3. The higher HDL cholesterol levels in the plasma of the coastline Chukot residents appears to reflect the higher cholesterol-scavenging capacity of their HDL. We conclude from this study that the regular consumption of dietary n-3 polyunsaturated fatty acids by the coastline Chukot residents decreased LDL cholesterol transfer from plasma to peripheral cells, and enhanced cholesterol efflux from cellular membranes toward HDL.

Fatty acids including saturated fatty acids also bind PUMA-G and HM74 receptors. This is the receptor family that Niacin binds to and exerts its potent abilities to regress plaque (raise HDL2b 200-300%, lower TGs 40-60%) and evoke its anti-inflammatory effects. See Table 1 full list of the range of ketone body and the saturated fatty acids and their relative receptor affinities.

Sunday, October 26, 2008

Received a call at the last minute from a co-worker offering a chance to run the Bothe-Napa State Park half-marathon that was sold out! My bib belonged to an Asian dude originally from South India (sshhhHHH! -- don't mention to the race owners). Scored a great workout (only 10K actually) and free cool wool socks...

The other trail running I've done was the Marin Headlands race a couple Aprils ago where the bluest-ever wildflowers were in a sea of blooms over magnificent green hills. Enviro-Sports does a fantastic job at picking breathtaking locales paired with perfect timing for optimum weather, temperature and picturesque views. Unlike the Marin Headlands, with the semi-drought we experienced here in Northern California, Bothe-Napa park had neither muddy streams nor any waist-deep creeks to cross *big grin* THANK GOD.

Here were the usual hazards associated with blazing through the forest at crazy breakneck speeds:--branches -- poking EXACTLY out at eye level--gravel, slippery dry leaves, uneven footing which promote face-plants, shin-plants and twisted ankles--steep slopes similar to downhill skiing (great place to catch your breath unless your foot catches a raised root or rock which can send you straight to the ground)--crossing shady creeks--TICKS - my main challenge (Lyme disease is indigenous -- needed to avoid petroleum skin/hair products which apparently ticks are highly attracted to)

My 6'2" race partner didn't need to worry as much about face-plants because I reassured him his face was definitely higher up from the ground than my vertically challenged one.

With all the senses heightened and exhilarated (trying strongly to avoid planting my head), it was difficult not to be totally captivated and distracted by the intoxicating smell of the forest and a particular aroma I couldn't quite identify until another runner shared with me that the woodsy perfume was (!) BAY LEAF (umbellularia californica). I've often cooked with it (the commercial Mediterrean species laurus nobilis) but the leaves were usually impotent and I've frankly never noticed anything so wonderful as what I was stomping and crunching below my feet. The air off the fresh leaves on the trees below the dense canopy wafted off as we brushed past them. Were the valleys just one big room deodorant? Could one possibly thrash the body any better while immersing the senses in this astonishingly sensual aromatherapeutic experience? (Honestly, a nice side effect of being on the an evolutionary/paleo lifestyle and diet is despite going through the gauntlet (Crossfit, endurance events, whatever), I rarely ever experience muscle aches or soreness afterwards. It defies bio-physics.)

My daughters love Pokemon and here is a creature they haven't discovered yet named after this fascinating spice:BAYLEEF

Bayleef (ベイリーフ, Beirīfu?, Bayleaf in original Japanese language versions) is the evolution of Chikorita and first appeared in Pokémon Gold and Silver. It has a pale yellow body supported by four legs and a rather long neck and tail. On top of its head is a single large leaf. Its most defining trait is the "necklace" of seven tubular leaves that is located around its neck. Each of these curled up leaves contains inside it a tree shoot. From these leaves wafts a spicy scent that has stimulating properties. It can cheer people up, restore their health, make them more energetic and even heighten their drive for competition.

Have you ever purchased bay leaves from the grocery spice aisle? One ounce costs more than M A R I J U A N A... j/k. Don't forget I'm a legal drug-dealer (ie, board-certified-doctor-of-pharmacy) . . . not the other. Seriously, the stuff we buy where the volatile oils (known as eugenol) are mostly degraded by storage and age doesn't hold anything against the REAL STUFF. After the race I wanted to go back and stuff leaves into my wet sweaty bra but I r e s i s t e d the urge I'm proud to tell y'll. State property after all!

Why did humans ever evolve cooking and spicing up our food with this wonderful herb? Why do the French tie bouquet garnis in their fragrant kitchens?? How did Greeks and ancient Romans find power in rewarding victors with wreaths of laurel/bay leaves? What do Indians and Persians favor in their biryani (rice)? Mexicans in their delish nutrish menudo?

Remarkable antimicrobial properties exist in all spices and herbs and bay leaves are no exception.

The first and only IPO I bought in high school was Calgene I'm sad to confess (f o o l I was...AND still am after missing GOOGLE). Talk about GMO-frankenfood monstrosities. *sigh* Perhaps, however, they've mildly redeemed themselves... somewhat. Their research on the California bay leaf enzyme called 12:0-ACP thioesterase shed light on it's involvement in lengthening the carbon chain in saturated fatty acids in the flowers (ie, seeds -- the reproductive parts) and leaves (less activity). Apparently the seeds of the California bay leaf tree are rich in lauric acid, the medium 12-carbon chain saturated fatty acid.

-- 16.7% for men (baseline: HDL = 1.26 mmol/L = 48.7 mg/dl) which appears to correlate well with Lp(a) reduction! Though hard to tell with Lp(a) varying in the deviations and this study population too small for any significance or actual comparisons.

In the below research conducted by the same group, they found that "Nevertheless, lipid transfer activities correlated significantly with the relative abundance of HDL2b, HDL2a, HDL3b, and HDL3c with phospholipid transfer activities. In general, serum phospholipid transfer protein (PLTP) activity correlated positivly with HDL cholesterol after the dietary interventions...serum PLTP activity, as measured as the rate of radiolabeled phosphatidylcholine transferred from liposomes toward serum HDL, was significantly higher with the lauric acid diet (23.5+/2.6%) than with the palmitic acid diet (22.5+/-2.5%) (P = 0.0013)."

Sunday, October 12, 2008

These Duke University cardiologists performed an RCT (randomized controlled trial) on exercise intensity and frequency and found that large big puffy HDLs are can be achieved with exercise and can be degraded by 'de-training'. They found "In conclusion, physical inactivity has profound negative effects on lipoprotein metabolism. Modest exercise prevented this. Moderate-intensity but not vigorous-intensity exercise resulted in sustained VLDL-triglyceride lowering. Thirty minutes per day of vigorous exercise, like jogging, has sustained beneficial effects on HDL metabolism."

Training consisted of a gradual increase in amount of exercise followed by 6 mo of exercise at the prescribed level. Exercise included treadmill, elliptical trainer, and stationary bicycle. The number of minutes necessary to expend the prescribed kilocalories per week (14 kcal x kg body wt(-1) x wk(-1) for both low-amount groups; 23 kcal x kg body wt(-1) x wk(-1) for high-amount group) was calculated for each subject. Average adherence was 83-92% for the three groups; minutes per week were 207, 125, and 203 and sessions per week were 3.6, 2.9, and 3.5 for high-amount/vigorous-intensity, low-amount/vigorous intensity, and low-amount/moderate-intensity groups, respectively. Plasma was obtained at baseline, 24 h, 5 days, and 15 days after exercise cessation.

A modest amount of exercise training prevented this deterioration (good).

Moderate-intensity but not vigorous-intensity exercise resulted in a sustained reduction in very-low-density lipoprotein (VLDL)-triglycerides over 15 days of detraining (P less than 0.05)

WOW. Yup not bad, eh? Moderate intensity was actually just as good the vigorous activity for reducing weight, in fact, was better for these untrained/sedentary individuals for de-training VLDL-TGs and body fat reducations. This is my experience as well -- I need long sustained, moderate intensity exercise to burn (stubborn) fat and maintain weight. Obviously the longer duration the better, and either intensities in the trial were better than nothing.Here the graph exemplifying the benefits of moderate intensity for belly fat reduction over vigorous intensity (see bottom bar graph). Low amounts of moderate produced a reduction of 1.2% subcutaneous belly fat compared with a 3.1% increase in the low amount vigorous group.Here the authors report the precise changes in body fat in the STRRIDE study Kraus WE et al J Appl Physiol 2005 Oct;99(4):1613-8: HERETheir conclusions from this analysis: "The equivalent of 11 miles of exercise per week, at either intensity, prevented significant accumulation of visceral fat. Controls gained visceral fat (8.6% BF +/- 17.2%; P = 0.001) in 6 months. Significant gains in visceral fat over only 6 mo emphasize the HIGH COST OF CONTINUED INACTIVITY. A modest exercise program, consistent with recommendations from the Centers for Disease Control/American College of Sports Medicine (CDC/ACSM), prevented significant increases in visceral fat." The highest exercise group lost ~ 7% body fat in only 8 months. Roughly approx one inch off the inches measured at our belly button (umbilical) is equivalent to approx 1% body fat. My personal experience mirrors these experimental measures. At moderate intensity which is equivalent to ~ 60% of our peak oxygen output, we our maximally in our aerobic fat-burning mode. Our muscles' (including the heart muscles) preferred energy source is fatty acids -- these are the longest burning 'logs' that fuel moving muscles. Sustained moderate intensity movement draws from our fat reserves the most optimally. Now, with that said, we do require a little intensity in life. My trainer once told me at the end of the workout, push the intensity to 70-80% for 1-2 minutes for speed and power later. Adding strength training and weights potentiates strength and burns visceral fat further (toxic fat enclosing our viscera/offal/organs, livers/gallbladders/hearts/etc). So minimum 11 miles per week? And for maximum gluteus maximus, squats + walking 20 miles per week?

The high-amount group had significant improvements in ALL the benefits below that were sustained for 15 daysafterexercise stopped:--high-density lipoprotein (HDL)-cholesterol--HDL particle size--large HDL levels

The more, the better the HDLs. Modest WALKING 10,000 steps most days... INTENSE PLAQUE BUSTING POWER!I like that. And the benefits can be sustained and uncompromised despite times when I can't get off my beautiful bum.

I really really really like T H A T .

Group Three is what we try to attain at the Track Your Plaque program at the mininum. But after conditioning and some practice, a moderate amount at moderate intensity is preferred for its lipoprotein-shifting, insulin-sensitizing, mood-elevating, stress-busting benefits.

Use a pedometer. Gradually work up to an ultimate goal of walking(not jogging) 10,000 steps per day. More details HERE at TYP.

We are not talking 'elite' athlete training or even amateur-weekend-athlete training. We are talking from an untrained, sedentary, have-not-exercised-since-Reagan-was-in-office perspective.

Aim to start LOW and go SLOW.

Take time to build up tendons, ligaments, strengthen joints and condition the lungs and other apparatus. Always warm up for the minumum 10-20 min in order to prevent injury or pulling a hamstring (my Achilles -- this used to frequently happen to me and derail training for 3-4mos -- but not now with squat exercises *smile* luv em). With the weather cooling now, warming up consistently and regularly will be the key to sustaining a program without disturbing injuries which would undoubtedly halt any well-intended program.

If you have not embarked on an exercise program before, then start first by asking your physician/cardiologist for an exercise stress Thallium to first assess flow, ischemia and changes on EKG. It is prudent for even well-trained elite athletes to undergo this test as well (as many have done and reported at the TYP forum) to make sure no underlying asymptomatic pathologies exist.

Saturday, October 11, 2008

~20-40+ per week (when genetics are not in your favor) I do a lot at Crossfit (hundreds) and at home... they are the BOMB for the B*TT Ladies and Gentlemen... And they prevent falls and hip fractures by strengthening the core muscles, gluts (ie, b*tt), hamstrings and quads. You'll love the results. Get strong. Do 'em. Do them correctly -- otherwise you'll be sorry and require knee surgery...

!!KEY!! -- Notice the position of keeping the front of your knee directly above the ankle (not ahead) -- and stick your SEXYBACK out as much as possible. Yea, it is a little obscene but don't worry I'm not watching.

Food composition can make a difference to what gains and benefits can be reaped. Researchers Volek et al at Penn State looked about how nutrients appear to modulate how high testosterone increases. Jumping squats produced higher testosterone than benching (more muscles more weight bearing involved). Experiment was conducted in men who have done resistance training for an average of 5 yrs and avg body fat (BF) was 13.3 %. Avg rep max for squats was 145 kg and for bench press 80 kg.

The present study examined the relationship between dietary nutrients and resting and exercise-induced blood concentrations of testosterone (T) and cortisol (C). Twelve men performed a bench press exercise protocol (5 sets to failure using a 10-repetitions maximum load) and a jump squat protocol (5 sets of 10 repetitions using 30% of each subject's 1-repetition maximum squat) with 2 min of rest between all sets. A blood sample was obtained at preexercise and 5 min postexercise for determination of serum T and C. Subjects also completed detailed dietary food records for a total of 17 days.

Just do it... Squat...Resistance Train... Here elite rugby players experience intense testosterone hormone surges with weight training to maximum repetition and repeat sets. Watch your sdLDL and Lp(a) drop as you reach your individual warrior potential. Reap benefits with REPS. Push it, I know you can do it. *wink* These researchers are good -- salivary is the way to go for testing.

The acute response of free salivary testosterone (T) and cortisol (C) concentrations to four resistance exercise (RE) protocols in 23 elite men rugby players was investigated. We hypothesized that hormonal responses would differ among individuals after four distinct RE protocols: four sets of 10 repetitions (reps) at 70% of 1 repetition maximum (1RM) with 2 minutes' rest between sets (4 x 10-70%); three sets of five reps at 85% 1RM with 3 minutes' rest (3 x 5-85%); five sets of 15 reps at 55% 1RM with 1 minute's rest (5 x 15-55%); and three sets of five reps at 40% 1RM with 3 minutes' rest (3 x 5-40%). Each athlete completed each of the four RE protocols in a random order on separate days. T and C concentrations were measured before exercise (PRE), immediately after exercise (POST), and 30 minutes post exercise (30 POST). Each protocol consisted of four exercises: bench press, leg press, seated row, and squats. Pooled T data did not change as a result of RE, whereas C declined significantly.

RESULTS:Individual athletes differed in their T response to each of the protocols, a difference that was masked when examining the pooled group data. When individual data were retrospectively tabulated according to the protocol in which each athlete showed the highest T response, a significant protocol-dependent T increase for all individuals was revealed.

CONCLUSION:Therefore, RE induced significant individual, protocol-dependent hormonal changes lasting up to 30 minutes after exercise. These individual responses may have important ramifications for modulating adaptation to RE and could explain the variability often observed in studies of hormonal response to RE.

This is the first that I've heard of statins inducing autoimmunity. But since food can (casein and wheat) why not statins?

Statin myopathy.Radcliffe KA, Campbell WW. Curr Neurol Neurosci Rep. 2008 Jan;8(1):66-72.Department of Neurology, Martin Army Community Hospital, 7950 Martin Loop, Fort Benning, GA 31905-5637, USA.
Many different classes of medications can cause toxic myopathy. One of the most frequently implicated classes is the statins. Statin myotoxicity ranges from asymptomatic creatine kinase elevations or myalgias to muscle necrosis and fatal rhabdomyolysis. Statins may also cause an autoimmune myopathy requiring immunosuppressive treatment. The mechanisms of statin myotoxicity are unclear. If unrecognized in its early manifestations, complications from continued statin therapy may lead to rhabdomyolysis and death. Risk factors for myotoxicity include concomitant medication use and medical conditions, and the patient's underlying genetic constitution. We review these considerations along with the recommended evaluation and treatment for patients presenting with statin myotoxicity.

Are the Lp(a) carriers superior with their resistance against scurvy, vitamin C deficiency, superiority against cancers/infections? Are these the mythical warrior race? The Amazonians?

Do they survive short-term life-sentences with no consequences...as long as they follow a 'warrior lifestyle'?--meat, milk, blood, organ meats, fish, seafood?--no grains? no refined carbs... ?--frequent high intensity battle, training?--frequent intermittent fasting?--stress control -- control of Type A and Type D tendencies?

It would appear so to me...

WCCA guy brings up Rath's theory on the TYP forum regarding multiple DNA breaks with scurvy and any other nutritional deficiencies to increase the DNA variations that would bring about EVOLUTION.

MetSyn also shown to be dangerous combination with Lp(a) as recognized by this researcher from Cairo, Egypt: Wassef GN.Lipoprotein (a) in android obesity and NIDDM: a new member in 'the metabolic syndrome'.Biomed Pharmacother. 1999 Dec;53(10):462-5. Review.PMID: 10665339

Ancient wheat afflicted ancient Egyptians as it afflicts us now: Nerlich AG, Rohrbach H, Zink A.[Paleopathology of ancient Egyptian mummies and skeletons. Investigations on the occurrence and frequency of specific diseases during various time periods in the necropolis of Thebes-West]Pathologe. 2002 Sep;23(5):379-85. Epub 2002 Aug 21. German.PMID: 12376865

All the literature from the race states breast cancer prevention is 'discovered'! But no mention of mod/high cholesterol, mod/high fats or low glycemic-index eating or vitamin D or fish oil or cruciferous veggies.

My wheat-whore/friend (who I *love/adore* and am trying to prevent her from killin herself-- has GRAVE's DISEASE) asked me did I bring my Gu?

HHHhhaaiilllll . . . N . . .O . . . I wanted a good race and good fun and absolutely no bonkin (though I hardly raised my basal heart rate -- maybe the next race). I had nut butter and a couple of eggs that morning. Some high-octane caffeine didn't hurt either.

Whole grains = WHOLE BALONEY

WHOLE grains = WHOLE breast cancer

...As Homer says... Duh...

Studies show in breast cancer HDL2 is low and HDL3 high -- wow... just like other proliferative and inflammatory processes like CAD (coronary artery disease).

Yes... was on $*&%$%@ levonorgestrel for the last ~5 yrs -- which screwed my HDL2b despite the vitamin D and high dose EPA+DHA I take. Synthetic hormones SUCK. Get off them -- as soon as possible and run. Bioidentical is the way to go. Or el naturel -- someone may be bare-foot and preggers soon. YIKES.

Low carb is not only preventive for breast cancer by raising HDL2 (and preventing MetSyn and chronic hyperinsulinemia), it's the way to go for better recovery, fitness, performance for prolonged endurance sports. Yes -- this is counter what athletes are pushed to traditionally do -- !!all those gels/carb-pasta LOADING--C-R-*-P. Our immune system is stronger without frequent carb-assaults. Don't underestimated the power of your immunity which plays a fantastic role in controlling cancer and inflammation. In endurance athletes, plasma concentrations of IL-6 (pro-inflammatory) and IL-10 (anti-inflammatory cytokines -- good stuff) were 2-foldgreater on the LOW carb trial than on the HIGH carb trial.